ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of the Chinese compound prescription Ginkgo biloba Pingchan Recipe (GBPR) on experimental Parkinson disease (PD) in mice and explore the possible mechanism.</p><p><b>METHODS</b>Male C57/BL6J mice were divided into normal control, PD model and treatment groups. PD model was established by intraperitoneal injection with 1-methl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP) in the mice, and in the treatment group, GBPR was administered intragastrically after the injection. The mice were sacrificed 14 and 28 days later, and using in situ hybridization with Digoxin-labeled nNOS cDNA oligonucleotide probe, neuronal nitric oxide synthase (nNOS) mRNA was detected in the striatum and substantia nigra in the brain of mice.</p><p><b>RESULTS</b>nNOS mRNA expression was detected in the striatum and substantia nigra of the PD model mice, and GBPR treatment significantly reduced its expressions.</p><p><b>CONCLUSION</b>GBPR has obvious inhibitory effect against the neurotoxicity of NO probably by producing an anti-oxiditive effect through decreasing nNOS synthesis in the brain.</p>
Subject(s)
Animals , Male , Mice , Brain , Metabolism , Disease Models, Animal , Drugs, Chinese Herbal , Pharmacology , Gene Expression Regulation, Enzymologic , Ginkgo biloba , Chemistry , Mice, Inbred C57BL , Neostriatum , Metabolism , Nitric Oxide Synthase Type I , Genetics , Parkinson Disease , Genetics , Metabolism , RNA, Messenger , Genetics , Metabolism , Substantia Nigra , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To explore the acting mechanism of Banxia Xiexin Decoction (BXD) and its disassembled recipes on stress gastric ulcer, for providing references to the scientific researches on the assembling rule of BXD.</p><p><b>METHODS</b>The rat model of acute gastric ulcer was established by water immersion-restraint stress. The experimental rats were divided into the normal group, the model group and the treated groups treated with BXD and its disassembled recipes respectively to observe the therapeutic efficacy and the changes of somatostatin (SS) expression in brain and gastric tissues.</p><p><b>RESULTS</b>In the model group, the SS expression was 0.0237 +/- 0.0056 in brain and 0.0171 +/- 0.0053 in gastric tissue respectively, which was significantly lower than those in the normal group (0.0305 +/- 0.0024 and 0.0282 +/- 0.0037) respectively. Compared to the model group, the two indexes in rats treated with full BXD were 0.0294 +/- 0.0050 and 0.0288 +/- 0.0027, treated with sweet flavor portion were 0.0314 +/- 0.0027 and 0.0219 +/- 0.0059, all showed increase of SS expression, and the increment was more significant in the former.</p><p><b>CONCLUSION</b>BXD can increase the expression of SS to realize its therapeutic efficacy, and the recipe was assembled rationally.</p>
Subject(s)
Animals , Male , Rats , Anti-Ulcer Agents , Therapeutic Uses , Immunohistochemistry , Phytotherapy , Plant Extracts , Chemistry , Therapeutic Uses , Random Allocation , Rats, Wistar , Somatostatin , Stomach Ulcer , Drug Therapy , Metabolism , Stress, PsychologicalABSTRACT
Current hypothesis of neuronal degeneration in Parkinson's disease (PD) have been proposed, including formation of free radicals and oxidative stress, mitochondrial dysfunction, excitotoxicity, trophic factor deficiency, inflammatory processes, genetic factors, environmental impact factors, toxic action of nitric oxide, apoptosis, and so on. This review mainly discussed oxidative stress, environmental impact factors, and inflammatory processes in PD.
Subject(s)
Animals , Humans , Environmental Pollutants , Inflammation , Allergy and Immunology , Oxidative Stress , Allergy and Immunology , Parkinson Disease , Allergy and ImmunologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanisms of Yinxing Pingchan recipe (YXPC) and its components, i.e. the components for detoxicating (A), for calming liver (B) and for dissolving blood stasis(C), in preventing and treating Parkinson's disease, and the path of its inhibition on nigrostriatal dopaminergic neuron (DAn) apoptosis in model mice of Parkinson's disease.</p><p><b>METHODS</b>Male C57BL/6J mice were divided into the normal group, the model group and four Chinese medicinal groups, that is, the YXPC group, and Group A, B and C, treated with YXPC and its components A, B and C respectively. Mouse model of Parkinson's disease was established by intraperitoneal injection with 1-methl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP). All mice were sacrificed in 2 batches at the 14th and the 28th day respectively. The activity of mitochondrial enzyme complex I, II and IV (MEC I, II and IV) in the brain of mice were measured, respectively.</p><p><b>RESULTS</b>As compared with the normal group, the activity of MEC I and IV in brain was significantly lower (P < 0.05 or P < 0.01), and that of MEC II had no obvious change in the model group. As compared with the model group, the activity of MEC I was significantly higher in YXPC group and Group C at the 14th day (P < 0.05), while the activity of MECII in Group A at the 14th day, Group B at the 28th day and Group C at both 14th and 28th day was significantly lower (P<0.05 or P<0.01). Activity of MEC IV in the four Chinese medicinal groups at the 14th day all significantly increased (P<0.05 or P<0.01), and retained at high level in Group B and Group C at the 28th day (P<0.05).</p><p><b>CONCLUSION</b>YXPC and its components can maintain the mitochondrial function by partial inhibiting the activity of its enzyme complex, preventing DAn apoptosis to slow down the progress of Parkinson's disease.</p>